The aim of this project is to identify the mechanisms responsible for the production of experimental allergic encephalomyelitis, a model of autoimmune disease which is manifested by demyelination. This disease is being studied in mice because this species is ideally suited for the analysis of immunologic and genetic factors which lead to disease. Three forms of the murine disease: 1) Acute Experimental Allergic Encephalomyelitis, 2) Chronic Relapsing Experimental Allergic Encephalomyelitis and 3) Adoptively Transferred Experimental Allergic Encephalomyelitis have been produced. Research is currently being focused on the adoptively transferred form of the disease. The transfer of lymphocytes sensitized against myelin basic protein leads to acute neurological dysfunction which is characterized pathologically by inflammation and primary demyelination. Many mice recover and develop chronic relapsing disease. The subpopulation of lymphocytes responsible for the transferred disease has been identified and the mechanisms related to the migration of immune cells across the blood brain barrier into the nervous system are being assessed. Interactions between immune cells and capillary endothelial cells are being studied.